EIF2AK2 and neoplasm: The precise mechanism for growth of ICP34.5 mutants in each tumour type is not fully understood, but it is known from knockout mouse studies that deletions and mutations in PKR and the IFN receptors allow ICP34.5 mutant growth (Leib et al, 1999, 2000), and that these mutations and deletions have been found in a number of tumour types (Haus, 2000).